Does early life exposure to iron represent a risk for Parkinson’s disease?
Brain iron increases with age; a phenomenon that is further accelerated in Parkinson’s disease.
Considering the relative impermeability of the blood-brain barrier to peripheral iron, it is unclear how and why this elevation in brain iron with age occurs, and why it is more pronounced in Parkinson’s disease. We hypothesise that key stages of brain development represent a critical window for maintaining healthy brain iron levels, and that iron overload in these periods increases the risk of age-related disease.
Aims
- Obtain baseline T2* MRI imaging of brains from living patients with Parkinson’s disease (PD) and relate to tooth iron concentration.
- Determine if early life iron exposure is correlated to the brain iron levels of the ageing brain
- Investigate if elevated brain iron levels in PD are a consequence in part of early life exposure or an independent disease-related event using early life dietary transitions as a marker of iron intake.
- Investigate if neurodegeneration observed in neonatal iron feeding models represents a suitable model for idiopathic PD that could potentially be arrested through iron chelation.
- Investigate if metal chelation will prevent neurodegeneration.
Hypothesis
Early life dietary intake of iron permanently elevates the brain iron content and thereby increases susceptibility to damage in ageing and parkinsonian neurodegeneration.
The permanent record of early life iron exposure in teeth can be related to adult brain iron concentration.
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